Evolution of inflammatory and immune reactions is dependent upon the recruitment and migration of circulating leukocytes to the site of injury or antigen deposition. The accumulation of leukocytes is dependent not only on chemotactic signals emanating from the inflammatory site, but also on the release of inflammatory mediators which enhance expression of adhesion molecules. Upregulation of adhesion molecules facilitates cell- matrix interactions to promote targeting of circulating cells to the lesion site. Recent evidence indicates that transforming growth factor beta provides an extremely potent signal for initiating a chemotactic response, and these studies have addressed the ability of TGF-beta to influence the requisite adhesion of leukocytes to endothelium and to extracellular matrix in their journey to the site of inflammation. Adhesion occurs through the expression of integrins which represent a family of cell surface proteins that mediate cell adhesion to other cells and to the extracellular matrix. The molecules have been shown to be vital to platelet aggregation, wound healing, immune activation, tissue repair and in tumor invasion.